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首页> 外文期刊>Life sciences >Nicotinic acetylcholine receptor stimulation impairs epidermal permeability barrier function and recovery and modulates cornified envelope proteins.
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Nicotinic acetylcholine receptor stimulation impairs epidermal permeability barrier function and recovery and modulates cornified envelope proteins.

机译：烟碱乙酰胆碱受体刺激损害表皮通透性屏障功能和恢复，并调节角化的包膜蛋白。

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To characterize how nicotinic acetylcholine receptors (nAChRs) influence epidermal barrier function and recovery following prolonged stress or direct nAChR activation or antagonism.Mice were subjected to psychological stress or treated topically with nAChR agonist or antagonist for 3 days. We assessed barrier permeability and recovery by measuring transepidermal water loss (TEWL) before and after barrier disruption. In parallel, we analyzed the production and localization of several epidermal cornified envelope proteins in mouse skin and in human EpiDerm? organotypic constructs stimulated with a nAChR agonist (nicotine) and/or a nAChR selective antagonist (α-bungarotoxin).We determined that psychological stress in mice impairs barrier permeability function and recovery, an effect that is reversed by application of the α7 selective nAChR antagonist, α-bungarotoxin (Bung). In the absence of stress, both topical nicotine or Bung treatment alone impaired barrier permeability. We further observed that stress, topical nicotine, or topical Bung treatment in mice influenced the abundance and/or localization of filaggrin, loricrin, and involucrin. Similar alterations in these three major cornified envelope proteins were observed in human EpiDerm? cultures.Perceived psychological stress and nicotine usage can both initiate or exacerbate several dermatoses by altering the cutaneous permeability barrier. Modulation of nAChRs by topical agonists or antagonists may be used to improve epidermal barrier function in skin diseases associated with defects in epidermal barrier permeability.
机译：表征烟碱乙酰胆碱受体（nAChRs）在长期应激或直接nAChR激活或拮抗后如何影响表皮屏障功能和恢复。将小鼠置于心理压力下或用nAChR激动剂或拮抗剂局部治疗3天。我们通过测量屏障破坏前后的表皮水分损失（TEWL）来评估屏障的通透性和恢复情况。同时，我们分析了小鼠皮肤和人类EpiDerm中几种表皮角质化包膜蛋白的产生和定位。通过nAChR激动剂（烟碱）和/或nAChR选择性拮抗剂（α-真菌毒素）刺激的器官型结构，α-真菌毒素（Bung）。在没有压力的情况下，单独的局部尼古丁或Bung治疗都会削弱屏障的通透性。我们进一步观察到，小鼠的压力，局部尼古丁或局部Bung处理会影响丝蛋白，loricrin和involucrin的丰度和/或位置。在人类EpiDerm？中观察到了这三种主要的玉米角化包膜蛋白的类似变化。感知的心理压力和尼古丁的使用可以通过改变皮肤的渗透性屏障来引发或加剧几种皮肤病。通过局部激动剂或拮抗剂对nAChRs的调节可用于改善与表皮屏障通透性缺陷相关的皮肤疾病中的表皮屏障功能。

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